OBJECTIVES: To determine the effects of passive leg raising (PLR) on hemodynamics and on cardiac function according to the preload dependency defined by the superior vena cava collapsibility index (DeltaSVC). RESULTS:Forty patients with shock, sedated and mechanically ventilated, were included. Transesophageal echocardiography was performed. At baseline (T1), two groups were defined according to DeltaSVC. Eighteen patients presenting a DeltaSVC > 36%, an indicator of preload dependency, formed group 1, whereas 22 patients (group 2) exhibited a DeltaSVC < 30% (not preload-dependent). Measurements were then performed during PLR (T2), back to baseline (T3), and after volume expansion (T4) in group 1 only. At T1, DeltaSVC was significantly higher in group 1 than in group 2, 50 +/- 9% and 7 +/- 6%, respectively. In group 1, we found a decrease in DeltaSVC at T2 (24 +/- 9%) and T4 (17 +/- 7%), associated with increased systolic, diastolic and arterial pulse pressures. Cardiac index also increased, from 1.92 +/- 0.74 (T1) to 2.35 +/- 0.92 (T2) and 2.85 +/- 1.2 l/min/m(2) (T4) and left ventricular end-diastolic volume from 51 +/- 41 to 61 +/- 51 and 73 +/- 51 ml/m(2). None of these variations was found in group 2. No change in heart rate was observed. CONCLUSION: Hemodynamic changes related to PLR were only induced by increased cardiac preload.
RCT Entities:
OBJECTIVES: To determine the effects of passive leg raising (PLR) on hemodynamics and on cardiac function according to the preload dependency defined by the superior vena cava collapsibility index (DeltaSVC). RESULTS: Forty patients with shock, sedated and mechanically ventilated, were included. Transesophageal echocardiography was performed. At baseline (T1), two groups were defined according to DeltaSVC. Eighteen patients presenting a DeltaSVC > 36%, an indicator of preload dependency, formed group 1, whereas 22 patients (group 2) exhibited a DeltaSVC < 30% (not preload-dependent). Measurements were then performed during PLR (T2), back to baseline (T3), and after volume expansion (T4) in group 1 only. At T1, DeltaSVC was significantly higher in group 1 than in group 2, 50 +/- 9% and 7 +/- 6%, respectively. In group 1, we found a decrease in DeltaSVC at T2 (24 +/- 9%) and T4 (17 +/- 7%), associated with increased systolic, diastolic and arterial pulse pressures. Cardiac index also increased, from 1.92 +/- 0.74 (T1) to 2.35 +/- 0.92 (T2) and 2.85 +/- 1.2 l/min/m(2) (T4) and left ventricular end-diastolic volume from 51 +/- 41 to 61 +/- 51 and 73 +/- 51 ml/m(2). None of these variations was found in group 2. No change in heart rate was observed. CONCLUSION: Hemodynamic changes related to PLR were only induced by increased cardiac preload.
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